Entry of Ca(2+) through voltage-dependent calcium channels (VDCCs) is critical to the regulation of intracellular free calcium concentration ([Ca(2+)](i)) in vascular smooth muscle and thus the control of cerebral artery diameter. Increased VDCC activity in cerebral artery myocytes may contribute to decreased cerebral blood flow and the accompanying neurological deficits associated with subarachnoid hemorrhage (SAH). This review will focus on the impact of SAH on VDCCs and K(+)-selective ion channels, two important classes of ion channels located in the plasma membrane of cerebral artery myocytes. SAH may act through a variety of direct and indirect mechanisms to increase the activity of VDCCs promoting cerebral artery constriction and reduced cerebral blood flow. Further, SAH may lead to suppression of K(+) channel activity to cause membrane potential depolarization to enhance VDCC activity. The ability of VDCC blockers or K(+) channel activators to alleviate SAH-induced vasospasm will also be examined.